ArticleProceedings of the National Academy of Sciences of the United States of America2011
Glucocorticoids target suppressor of cytokine signaling 1 (SOCS1) and type 1 interferons to regulate Toll-like receptor-induced STAT1 activation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 91 citations in OpenAlex.
- Network analysis identifies a putative role for the PPAR and type 1 interferon pathways in glucocorticoid actions in asthmatics.BMC medical genomics · 2012Trial
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- Age-Specific Considerations in Bronchiectasis Management: Focus on Older Adults with Emphasis on Anti-inflammatory Treatment.Drugs & aging · 2026Review
- Molecular Simulation-Based Insights into the Pharmacological Role of Silk Fibroin in Peripheral Nerve Repair.ACS chemical neuroscience · 2025Article
- Single cell analysis identified IFN signaling activation contributes to the pathogenesis of pediatric steroid-sensitive nephrotic syndrome.Biomarker research · 2025Article
- Exploring precision treatments in immune-mediated inflammatory diseases: Harnessing the infinite potential of nucleic acid delivery.Exploration (Beijing, China) · 2025Review
- Regulation of inflammatory pathways by cannabigerol in the collagen induced arthritis model in rats.Frontiers in pharmacology · 2025Article
- Omega-3 fatty acid synergy with glucocorticoid in mouse lupus macrophage model: targeting pathogenic pathways to reduce steroid dependence.Frontiers in immunology · 2025Article
- Dose-Dependent Glucocorticoid Regulation of Transcription Factors in Vocal Fold Fibroblasts and Macrophages.The Laryngoscope · 2023Article
- T Cell Energy Metabolism Is a Target of Glucocorticoids in Mice, Healthy Humans, and MS Patients.Cells · 2023Article
- Dexamethasone impairs the expression of antimicrobial mediators in lipopolysaccharide-activated primary macrophages by inhibiting both expression and function of interferon β.Frontiers in immunology · 2023Article
- Physiological Convergence and Antagonism Between GR and PPARγ in Inflammation and Metabolism.Advances in experimental medicine and biology · 2022Review
- Zinc inhibits lethal inflammatory shock by preventing microbe-induced interferon signature in intestinal epithelium.EMBO molecular medicine · 2020Article
- COVID-19 Patients Upregulate Toll-like Receptor 4-mediated Inflammatory Signaling That Mimics Bacterial Sepsis.Journal of Korean medical science · 2020Article
- Dynamics of the Type I Interferon Response During Immunosuppressive Therapy in Rheumatoid Arthritis.Frontiers in immunology · 2019Article
- Higher activation of the interferon-gamma signaling pathway in systemic lupus erythematosus patients with a high type I IFN score: relation to disease activity.Clinical rheumatology · 2018Article
- Glucocorticoid receptor dimers control intestinal STAT1 and TNF-induced inflammation in mice.The Journal of clinical investigation · 2018Article
- Kudzu Leaf Extract Suppresses the Production of Inducible Nitric Oxide Synthase, Cyclooxygenase-2, Tumor Necrosis Factor-Alpha, and Interleukin-6 via Inhibition of JNK, TBK1 and STAT1 in Inflammatory Macrophages.International journal of molecular sciences · 2018Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Endogenous and pharmacologic glucocorticoids (GCs) limit inflammatory cascades initiated by Toll-like receptor (TLR) activation. A long-standing clinical observation has been the delay between GC administration and the manifestation of GC's anti-inflammatory actions. We hypothesized that the GCs would have inhibitory effects that target late temporal pathways that propagate proinflammatory signals. Here we interrogated signal transducer and activator of transcription 1 (STAT1) regulation by GC and its consequences for cytokine production during activation of macrophages with TLR-specific ligands. We found that robust STAT1 activation does not occur until 2-3 h after TLR engagement, and that GC suppression of STAT1 phosphorylation first manifests at this time. GC attenuates TLR4-mediated STAT1 activation only through induction of suppressor of cytokine signaling 1 (SOCS1), which increases throughout the 6-h period after treatment. Inhibition of TLR3-mediated STAT1 activation occurs via two mechanisms, impairment of type I IFN secretion and induction of SOCS1. Our data show that SOCS1 and type I interferons are critical GC targets for regulating STAT1 activity and may account for overall GC effectiveness in inflammation suppression in the clinically relevant time frame.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.